Role of Carbonic Anhydrase in Cerebral Ischemia and Carbonic Anhydrase Inhibitors as Putative Protective Agents.


Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
10 May 2021
Historique:
received: 28 04 2021
revised: 07 05 2021
accepted: 07 05 2021
entrez: 2 6 2021
pubmed: 3 6 2021
medline: 16 6 2021
Statut: epublish

Résumé

Ischemic stroke is a leading cause of death and disability worldwide. The only pharmacological treatment available to date for cerebral ischemia is tissue plasminogen activator (t-PA) and the search for successful therapeutic strategies still remains a major challenge. The loss of cerebral blood flow leads to reduced oxygen and glucose supply and a subsequent switch to the glycolytic pathway, which leads to tissue acidification. Carbonic anhydrase (CA, EC 4.2.1.1) is the enzyme responsible for converting carbon dioxide into a protons and bicarbonate, thus contributing to pH regulation and metabolism, with many CA isoforms present in the brain. Recently, numerous studies have shed light on several classes of carbonic anhydrase inhibitor (CAI) as possible new pharmacological agents for the management of brain ischemia. In the present review we summarized pharmacological, preclinical and clinical findings regarding the role of CAIs in strokes and we discuss their potential protective mechanisms.

Identifiants

pubmed: 34068564
pii: ijms22095029
doi: 10.3390/ijms22095029
pmc: PMC8126098
pii:
doi:

Substances chimiques

Bicarbonates 0
Carbonic Anhydrase Inhibitors 0
Sulfonamides 0
Carbon Dioxide 142M471B3J
Carbonic Anhydrases EC 4.2.1.1

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Ministero dell'Istruzione, dell'Università e della Ricerca
ID : 2017XYBP2R

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Auteurs

Irene Bulli (I)

Department of Neuroscience, Psycology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.

Ilaria Dettori (I)

Department of Neuroscience, Psycology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.

Elisabetta Coppi (E)

Department of Neuroscience, Psycology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.

Federica Cherchi (F)

Department of Neuroscience, Psycology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.

Martina Venturini (M)

Department of Neuroscience, Psycology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.

Lorenzo Di Cesare Mannelli (L)

Department of Neuroscience, Psycology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.

Carla Ghelardini (C)

Department of Neuroscience, Psycology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.

Alessio Nocentini (A)

Department of Neuroscience, Psycology, Drug Research and Child Health (NEUROFARBA), Section of Pharmaceutical Sciences, University of Florence, 50019 Florence, Italy.

Claudiu T Supuran (CT)

Department of Neuroscience, Psycology, Drug Research and Child Health (NEUROFARBA), Section of Pharmaceutical Sciences, University of Florence, 50019 Florence, Italy.

Anna Maria Pugliese (AM)

Department of Neuroscience, Psycology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.

Felicita Pedata (F)

Department of Neuroscience, Psycology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.

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